by Noelle La Croix, DVM, Dip. ACVO
Uveitis – Treatment
In two previous articles, I discussed the nature of uveitis and its diagnosis. In this final article of this series, I want to discuss the treatment of uveitis. Treatments involve appropriate medications, follow-up evaluations of medicinal efficacy, and ultimately the tapering of medications as clinical signs resolve.
The ultimate goal of uveitis therapy is the total regression of white blood cells and protein from within the anterior chamber and the re-stabilization of the blood-ocular barrier. The regression of uveitis is therefore most directly measured by the elimination of aqueous flare. Flare indicates that the blood-ocular barrier has broken down and vascular spaces are leeching proteins and/or cells into the anterior chamber. Aqueous flare is most accurately visualized with a slit lamp microscope. Other clinical signs of persistent uveitis include miosis, conjunctival hyperemia, scleral injection, rubeosis irides, and decreased intraocular pressure.
Uveitis is typically treated with both oral and topical corticosteroids to control and ultimately resolve inflammation. Corticosteroids mediate their anti-inflammatory effects through the modulation of cytoplasmic glucocorticoid receptors. Corticosteroids bind receptors forming active complexes that migrate to the nucleus. These complexes then increase expression of anti-inflammatory proteins and repress the expression of pro-inflammatory proteins. Topical (ocular) administration generates higher concentration of steroids within the anterior chamber than systemic administration. Typically, most cases of uveitis are initially treated with both oral and topical medications to repress the entire immune system. Systemic steroids are also particularly necessary in cases of posterior uveitis, as drops of ocular steroids do not effectively reach the vitreous chamber and chorioid.
The topical steroids that effectively penetrate the cornea and reach the anterior chamber include 1% prednisolone acetate, and 0.1% dexamethasone (often prescribed in a preparation containing neomycin and polymyxin B) (Figure 1). Suspensions of these drugs need to be shaken before ocular application to assure proper dosing. Based upon pharmokinetic studies, prednisolone acetate is slightly more effective controlling inflammation when compared with dexamethasone. The pharmokinetics of both generic (Falcon Pharmaceuticals) or branded (Alcon’s Omnipred) prednisolone acetate have been particularly improved by decreasing the drug’s particulate size. Unfortunately, prednisolone acetate can also be systemically absorbed through conjunctival vasculature and/or the nasal mucosa (via nasolacrimal ducts). This absorption can cause polydipsia and polyuria, particularly in smaller animals (less than 4.5 kg). Non-steroidal anti-inflammatories (flurbiprofen, diclofenac) or neomycin-polymyxin B-dexamethasone are therefore preferable to prednisolone acetate for treating the uveitis of smaller animals. The hydrocortisone found in some triple antibiotic preparations will not penetrate the cornea, and is therefore inappropriate for treating uveitis.
In the treatment of uveitis, atropine is prescribed to prevent miosis (with secondary posterior synechiae) and spasms of the ciliary body. Pupillary dilation will tamponade iridal vasculature, reduce the surface area of the iris, and prevent endothelial leakage of the uvea. Atropine is prescribed in all cases of uveitis, unless concurrent glaucoma is present. A side-effect of atropine is decreased tear production, necessitating the monitoring and management of the tear film.
Systemic anti-inflammatories are typically prescribed at 0.5 to 1.0 mg/kg by mouth twice daily. These medications should be tapered over time to use minimal dosages as uveitis regresses. Systemic anti-inflammatories will counter uveal inflammation but can also immunosuppress patients over time. It is therefore important to carefully monitor and taper these drugs appropriately.
In addition to topical and oral steroids, the underlying causes of uveitis can also often be effectively treated. For example, oral doxycycline can be prescribed if tick-borne diseases or Bartonella (in cats) are suspected of causing the uveitis. Ultimately, determining the root cause of a case of uveitis, followed by appropriate treatments, will help prevent subsequent uveitis.
Uveitis requires aggressive treatments to prevent ocular damage and a possible loss of vision. The immunomodulating drugs prescribed to treat uveitis must be carefully monitored for efficacy and unwanted side-effects. The etiologies of uveitis are actively researched and this will probably lead to more specific drugs in the future. If you have further questions about the treatment of uveitis, please consult with a veterinary ophthalmologist.
Noelle La Croix, DVM, Dip. ACVO
Veterinary Medical Center of Long Island
75 Sunrise Highway
West Islip, New York 11795
(631) 587-0800; fax (631) 587-2006
Figure 1: Medications that are used to control uveitis.